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Antioxidants
Special Issues
Oxidative Stress in Eye Diseases
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Oxidative Stress in Eye Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 3754

Special Issue Editors

Prof. Dr. Dhirendra Pratap Singh

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Guest Editor
Ophthalmology and Visual Sciences, University of Nebraska medical Center, Omaha, NE 68198, USA
Interests: aging and oxidative stress; antioxidants; reactive oxygen species and molecular signaling; small molecules and therapeutic targets; redox mechanisms and gene regulation
Dr. Eri Kubo

E-Mail Website
Guest Editor
Department of Ophthalmology, Kanazawa Medical University, Kahoku District, Ishikawa, Japan
Interests: cataract; posterior capsular opacification; oxidative stress; epithelial-to mesenchymal transition; antioxidant; antiglycation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent pioneering research in redox biology has enhanced our comprehension of the role of reactive oxygen species (ROS)-induced oxidative stress in aging, as the deterioration of the cellular antioxidant defense system is a significant contributor to the development of visual impairments such as glaucoma, age-related macular degeneration, and cataracts. Nevertheless, despite a wealth of information demonstrating the role of oxidative stress in the induction of aging-related blinding diseases, the molecular mechanisms involved in the onset of oxidative-induced pathology are poorly understood. Also, the causes for excessive intracellular ROS production and dysregulation of the antioxidant defense system, leading to different types of cell death, like apoptosis, pyroptosis, ferroptosis, and so on, and their connection to ocular pathologies, remain elusive. Thus, there is a need to delineate the molecular mechanisms involved between oxidative stress and cell death types and identify the responsible culprit factors(s) to develop target-based therapeutics.

This Special Issue of Antioxidants will focus on studies on unveiling the molecular mechanism of oxidative stress/aging-induced pathological signaling and identify the involved culprit factors causing onset of ocular pathology for a structured tailored approach to manage or treat oxidative-/age-related blinding disorders.

Prof. Dr. Dhirendra Pratap Singh
Dr. Eri Kubo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxidative stress
  • antioxidants
  • reactive oxygen species
  • redox signaling, inflammatory cell death
  • age-related blinding diseases
  • glaucoma
  • cataract
  • age-related macular degeneration
  • gene regulation
  • retinal disorder
  • dry eye disorder
  • corneal diseases

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Published Papers (3 papers)

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Research

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27 pages, 3515 KiB  
Article
Antioxidant Activity and Cytotoxicity Evaluation of New Catechol Hydrazinyl-Thiazole Derivatives as Potential Protectors in Retinal Degenerative Processes
by Răzvan-Geo Antemie, Gabriel Marc, Raluca Pele, Ionel Fizeșan, Ionuț-Valentin Creștin, Raluca Borlan, Panagiotis Theodosis-Nobelos, Eleni A. Rekka, Ovidiu Oniga, Ovidiu Crișan, Adrian Pîrnău, Laurian Vlase and Simona Valeria Clichici
Antioxidants 2025, 14(6), 646; https://doi.org/10.3390/antiox14060646 - 28 May 2025
Viewed by 1516
Abstract
Retinal degenerative processes such as age-related macular degeneration are at the center of many ongoing research studies, as their impact on the general population is significant, with severe visual impairment and even irreversible vision loss if left untreated. Currently, there are few efficient [...] Read more.
Retinal degenerative processes such as age-related macular degeneration are at the center of many ongoing research studies, as their impact on the general population is significant, with severe visual impairment and even irreversible vision loss if left untreated. Currently, there are few efficient treatments available to stop or limit its progression. In the present paper, a molecular hybridization approach was employed to develop novel compounds that address this issue. By adding either 2-butenal or a β-ionone-derived residue to the hydrazone-catechol-thiazole scaffold, two compounds were designed and synthesized: 5a and 5b. After being characterized by mass spectrometry and nuclear magnetic resonance, and proving potent antioxidant activity in the in vitro assays, the cytotoxicity evaluation using the ARPE-19, BJ, and A549 cell lines revealed a surprisingly low-dose effect of 5a and the unexpected cytotoxic activity of 5b, despite its β-ionone moiety, known for its significant therapeutic properties. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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19 pages, 6004 KiB  
Article
Resveratrol Protects Photoreceptors in Mouse Models of Retinal Degeneration
by Shujuan Li, Hongwei Ma and Xi-Qin Ding
Antioxidants 2025, 14(2), 154; https://doi.org/10.3390/antiox14020154 - 28 Jan 2025
Viewed by 1127
Abstract
Photoreceptor/retinal degeneration is the major cause of blindness. Induced and inherited mouse models of retinal degeneration are valuable tools for investigating disease mechanisms and developing therapeutic interventions. This study investigated the potential of the antioxidant resveratrol to relieve photoreceptor degeneration using mouse models. [...] Read more.
Photoreceptor/retinal degeneration is the major cause of blindness. Induced and inherited mouse models of retinal degeneration are valuable tools for investigating disease mechanisms and developing therapeutic interventions. This study investigated the potential of the antioxidant resveratrol to relieve photoreceptor degeneration using mouse models. Clinical studies have shown a potential association between thyroid hormone (TH) signaling and age-related retinal degeneration. Excessive TH signaling induces oxidative stress/damage and photoreceptor death in mice. C57BL/6 (rod-dominant) and Nrl−/− (cone-dominant) mice at postnatal day 30 (P30) received triiodothyronine (T3) via drinking water (20 µg/mL) with or without concomitant treatment with resveratrol via drinking water (120 µg/mL) for 30 days, followed by evaluation of photoreceptor degeneration, oxidative damage, and retinal stress responses. In experiments using Leber congenital amaurosis model mice, mother Rpe65−/− and Rpe65−/−/Nrl−/− mice received resveratrol via drinking water (120 µg/mL) for 20 days and 10–13 days, respectively, beginning on the day when the pups were at P5, and pups were then evaluated for cone degeneration. Treatment with resveratrol significantly diminished the photoreceptor degeneration induced by T3 and preserved photoreceptors in Rpe65-deficient mice, manifested as preserved retinal morphology/outer nuclear layer thickness, increased cone density, reduced photoreceptor oxidative stress/damage and apoptosis, reduced upregulation of genes involved in cell death/inflammatory responses, and reduced macroglial cell activation. These findings demonstrate the role of oxidative stress in photoreceptor degeneration, associated with TH signaling and Rpe65 deficiency, and support the therapeutic potential of resveratrol/antioxidants in the management of retinal degeneration. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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Review

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29 pages, 1416 KiB  
Review
Restoring Glutathione Homeostasis in Glycation-Related Eye Diseases: Mechanistic Insights and Therapeutic Interventions Beyond VEGF Inhibition
by Yong Chool Boo
Antioxidants 2025, 14(6), 731; https://doi.org/10.3390/antiox14060731 - 14 Jun 2025
Viewed by 475
Abstract
Advanced glycation end-products (AGEs) and oxidative stress are recognized as central contributors to the pathogenesis of age-related or diabetic cataracts, diabetic retinopathy (DR), and age-related macular degeneration (AMD). These glycation-related diseases are characterized by impaired redox balance and decreased glutathione (GSH) levels. This [...] Read more.
Advanced glycation end-products (AGEs) and oxidative stress are recognized as central contributors to the pathogenesis of age-related or diabetic cataracts, diabetic retinopathy (DR), and age-related macular degeneration (AMD). These glycation-related diseases are characterized by impaired redox balance and decreased glutathione (GSH) levels. This review aims to examine the mechanistic links between AGEs and GSH depletion across ocular tissues by integrating in vitro, ex vivo, in vivo, and clinical studies relevant to this topic. The multiple levels of evidence highlight GSH homeostasis as both a biomarker and therapeutic target in glycation-related ocular disorders. Therapeutic strategies aimed at restoring GSH homeostasis under glycation stress are categorized into four mechanistic domains: (I) promoting GSH supply and synthesis, (II) enhancing GSH recycling, (III) mitigating glycation stress, and (IV) reducing oxidative and nitrosative stress. Most of these strategies have been explored via different approaches, and experimental findings with various interventions have shown promise in restoring GSH balance and mitigating AGE-induced damage. A pathological link between GSH depletion and vascular endothelial growth factor (VEGF) overexpression is observed in DR and wet AMD. GSH-centered interventions act upstream to modulate redox homeostasis while anti-VEGF therapies target downstream angiogenesis. This study supports the rationale for a dual-targeting strategy that combines redox-based interventions with VEGF inhibition in glycation-related ocular diseases. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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